Search results for "Channel blocker"

showing 10 items of 157 documents

Arginine vasopressin, via activation of post-junctional V1 receptors, induces contractile effects in mouse distal colon

2013

The aim of this study was to analyze whether arginine vasopressin (AVP) may be considered a modulator of intestinal motility. In this view, we evaluated, in vitro, the effects induced by exogenous administration of AVP on the contractility of mouse distal colon, the subtype(s) of receptor(s) activated and the action mechanism. Isometric recordings were performed on longitudinal and circular muscle strips of mouse distal colon. AVP (0.001 nM-100 nM) caused concentration-dependent contractile effects only on the longitudinal muscle, antagonized by the V1 receptor antagonist, V-1880. AVP-induced effect was not modified by tetrodotoxin, atropine and indomethacin. Contractile response to AVP was…

AtropineMaleReceptors Vasopressinmedicine.medical_specialtyVasopressinCarbacholNifedipineColonPhysiologyIndomethacinClinical BiochemistryMuscarinic AntagonistsTetrodotoxinCholinergic AgonistsIn Vitro TechniquesBiologyBiochemistryContractilityMiceCellular and Molecular Neurosciencechemistry.chemical_compoundPhosphoinositide Phospholipase CEndocrinologyInternal medicinemedicineAnimalsCyclooxygenase InhibitorsReceptorVasopressin receptorPhospholipase CArginine vasopressin receptor 1AMuscle SmoothCalcium Channel BlockersArginine vasopressinIntestinalcontractility V1 receptorsPhospholipase C Mouse colonArginine VasopressinEnzyme ActivationMice Inbred C57BLEndocrinologychemistryCarbacholGastrointestinal MotilityCyclopiazonic acidhormones hormone substitutes and hormone antagonistsMuscle ContractionSignal Transductionmedicine.drugRegulatory Peptides
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Mode and mechanism of neurotensin action in rat proximal colon

1997

Abstract This study examined the mechanism of action of neurotensin on intraluminal pressure in rat proximal colon. The direct and indirect contractile response to neurotensin (100 nM) was abolished in Ca 2+ -free solution, and was antagonized by nifedipine (1–5–10 nM) and potentiated by Bay K 8644 (methyl 1,4-dihydro-2,6-dimethyl-3-nitro-4-(2-trifluoromethylphenyl)-pyridine-5-carboxylate) (10–100–1000 nM). Neurotensin, in the presence of nifedipine (10 nM) and atropine (1 μM), induced a tetrodotoxin-insensitive inhibitory effect, which was antagonized by SR 48692 (2[(1-(7-chloro-4-quinolinyl)-5-(2,6-dimethoxy-phenyl)pyrazol-3-yl) carbonyl amino]tricyclo (3.3.1.1. 3.7 ) decan-2-carboxylic a…

Atropinemedicine.medical_specialtyNifedipineColonchemistry.chemical_elementCholinergic AgonistsIn Vitro TechniquesCalciumInhibitory postsynaptic potentialApaminCholinergic Antagonistschemistry.chemical_compoundNifedipineInternal medicinemedicineAnimalsReceptors NeurotensinRats WistarNeurotensinPharmacologyChemistryMuscle Smooth3-Pyridinecarboxylic acid 14-dihydro-26-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)- Methyl esterBethanecholCalcium Channel BlockersRatsCalcium Channel AgonistsEndocrinologyApaminMechanism of actionQuinolinesExcitatory postsynaptic potentialBiophysicsPyrazolesCalciummedicine.symptomMuscle Contractionmedicine.drugMuscle contractionNeurotensinEuropean Journal of Pharmacology
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Role of calcium in E-selectin induced phenotype of T84 colon carcinoma cells

2003

The adhesion of cancer cells to the endothelium during the metastatic process involves the interaction of specific cell-cell adhesion receptors on the cell surface. E-selectin on endothelial cells and sialyl Lewis X carbohydrate component on tumor cells are mainly implicated in the adhesion of colon carcinoma cells to the endothelium of target organ. In this paper we show that binding of E-selectin to T84 colon tumor cells causes approximately a twofold increase in intracellular calcium concentration. In particular, using two inhibitors of receptor operated calcium channels, CAI and SK&F 96365, we present evidences that the augmentation in cytoplasmic calcium originates from ionic influx fr…

BiophysicsAntineoplastic AgentsCD38BiochemistryCalcium in biologyCell MovementE-selectinTumor Cells CulturedHumansCalcium SignalingPhosphorylationCell adhesionMolecular BiologyCalcium signalingbiologyImidazolesCell BiologyTriazolesCalcium Channel BlockersRecombinant ProteinsCell biologyPhenotypeColonic NeoplasmsCancer cellbiology.proteinTyrosineCalciumNeural cell adhesion moleculeSignal transductionE-SelectinBiochemical and Biophysical Research Communications
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Role of NO-synthases and cyclooxygenases in the hyperreactivity of male rabbit carotid artery to testosterone under experimental diabetes.

2009

Abstract Cardiovascular disease is the major cause of morbidity and mortality in diabetic patients, which in turn is also associated with low levels of serum testosterone. The working hypothesis was that diabetes might modify the mechanisms involved in the vascular actions of testosterone in isolated rabbit carotid arteries. Testosterone (10 −8 –3 × 10 −4  M) induced a concentration-dependent relaxation of precontracted carotid arteries, which was higher in diabetic than in control rabbits. In control rabbits neither endothelium removal nor the nitric oxide synthase (NOS) inhibitor N G -nitro- l -arginine ( l -NOArg, 10 −5  M) modified the relaxant action of testosterone, and the cyclooxyge…

Blood GlucoseCarotid Artery DiseasesMalemedicine.medical_specialtyArginineEndotheliumCharybdotoxinNitric Oxide Synthase Type IIIThromboxaneBlotting WesternIndomethacinNitric Oxide Synthase Type IIVasodilationProstacyclinNitric OxideNitroarginineDiabetes Mellitus ExperimentalImmunoenzyme TechniquesThromboxane A2Internal medicinemedicinePotassium Channel BlockersAnimalsCyclooxygenase InhibitorsTestosteronePharmacologybiologyDose-Response Relationship Drugbusiness.industryTestosterone (patch)EpoprostenolNitric oxide synthaseVasodilationEndocrinologymedicine.anatomical_structureCarotid ArteriesApaminCyclooxygenase 2cardiovascular systembiology.proteinPotassiumCalciumCyclooxygenaseEndothelium VascularRabbitsbusinessDiabetic Angiopathiesmedicine.drugPharmacological research
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Mechanisms involved in the relaxant action of testosterone in the renal artery from male normoglycemic and diabetic rabbits.

2009

Kidney disease is a frequent complication in diabetes, and significant differences have been reported between male and female patients. Our working hypothesis was that diabetes might modify the vascular actions of testosterone in isolated rabbit renal arteries and the mechanisms involved in these actions. Testosterone (10(-8) to 10(-4)M) induced relaxation of precontracted arteries, without significant differences between control and diabetic rabbits. Both in control and diabetic rabbits endothelium removal inhibited testosterone relaxant action. In arteries with endothelium, incubation with indomethacin (10(-5)M), N(G)-nitro-l-arginine (10(-5)M) or tetraethylammonium (10(-5)M) did not modi…

Blood GlucoseMalemedicine.medical_specialtyEndotheliumNitric Oxide Synthase Type IIIThromboxaneBlotting WesternIndomethacinNitric Oxide Synthase Type IIProstacyclinVasodilationNitroarginineMuscle Smooth VascularDiabetes Mellitus ExperimentalImmunoenzyme TechniquesThromboxane A2Renal ArteryEnosInternal medicinemedicine.arteryDiabetes mellitusmedicinePotassium Channel BlockersAnimalsCyclooxygenase InhibitorsProstaglandins ITestosteroneRenal arteryPharmacologybiologyDose-Response Relationship Drugbusiness.industryTetraethylammoniumTestosterone (patch)medicine.diseasebiology.organism_classificationVasodilationEndocrinologymedicine.anatomical_structureCyclooxygenase 2Cyclooxygenase 1PotassiumCalciumEndothelium VascularRabbitsbusinessmedicine.drugSignal TransductionPharmacological research
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MitoKATP-channel opener protects against neuronal death in rat venous ischemia.

2005

OBJECTIVE: Mitochondrial adenosine triphosphate-dependent potassium (mitoK ATP ) channels are present in the brain, and several reports have shown their neuroprotective, preconditioning effect against an ischemic insult. The role of mitoK ATP channels in the penumbra area has not been studied thoroughly. In a model of venous ischemia, widespread penumbra-like low flow areas are created, which are susceptible to cortical spreading depression. Thus, we studied effects of mitoK ATP channels on infarct size in this model. METHODS: Male Wistar rats were subjected to two-vein occlusion by photochemical thrombosis of two adjacent cortical veins combined with KCI-induced cortical spreading depressi…

Brain InfarctionMalemedicine.medical_specialtyPotassium ChannelsPhotochemistryIschemiaBrain EdemaPotassium ChlorideIschemiaInternal medicinemedicineDiazoxideLaser-Doppler FlowmetryAnimalsChannel blockerDrug InteractionsRats WistarNeuronsAnalysis of VarianceCell Deathbusiness.industryPenumbraCortical Spreading DepressionDiazoxidemedicine.diseaseCerebral VeinsPotassium channelRatsTolerance inductionDisease Models AnimalNeuroprotective AgentsCerebral blood flowRegional Blood FlowAnesthesiaCortical spreading depressionCardiologySurgeryNeurology (clinical)businessHydroxy AcidsAnti-Arrhythmia AgentsDecanoic Acidsmedicine.drugNeurosurgery
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MS4A12 is a colon-selective store-operated calcium channel promoting malignant cell processes.

2008

AbstractUsing a data mining approach for the discovery of new targets for antibody therapy of colon cancer, we identified MS4A12, a sequence homologue of CD20. We show that MS4A12 is a cell surface protein. Expression analysis and immunohistochemistry revealed MS4A12 to be a colonic epithelial cell lineage gene confined to the apical membrane of colonocytes with strict transcriptional repression in all other normal tissue types. Expression is maintained upon malignant transformation in 63% of colon cancers. Ca2+ flux analyses disclosed that MS4A12 is a novel component of store-operated Ca2+ entry in intestinal cells. Using RNAi-mediated gene silencing, we show that loss of MS4A12 in LoVo co…

Calcium Channel Blockers/pharmacologyCancer ResearchColorectal cancerColonCalcium Channels/geneticsCell Differentiation/geneticsEpidermal Growth Factor/pharmacologyBiologyRNA Small Interfering/pharmacologyModels BiologicalMalignant transformationEpidermal growth factorCell Line TumormedicineMembrane Proteins/antagonists & inhibitorsHumansGrowth factor receptor inhibitorNeoplasm InvasivenessRNA Small InterferingEpidermal Growth FactorGene Expression ProfilingMembrane ProteinsColonic Neoplasms/geneticsCell DifferentiationApical membranemedicine.diseaseCalcium Channel BlockersColon/metabolismCell biologyChemokines/metabolismProtein Structure TertiaryGene Expression Regulation NeoplasticOncologyCell cultureOrgan SpecificityCancer cellColonic NeoplasmsDisease ProgressionCalcium ChannelsChemokinesA431 cellsCancer research
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Excitotoxic Hippocampal Membrane Breakdown and its Inhibition by Bilobalide: Role of Chloride Fluxes

2003

We have previously shown that hypoxia and N-methyl-D-aspartate (NMDA) receptor activation induce breakdown of choline-containing phospholipids in rat hippocampus, a process which is mediated by calcium influx and phospholipase A (2) activation. Bilobalide, a constituent of Ginkgo biloba, inhibited this process in a potent manner (Weichel et al., Naunyn-Schmiedeberg's Arch. Pharmacol. 360, 609-615, 1999). In this study, we used fluorescence microscopy and radioactive flux measurements to show that bilobalide does not interfere with NMDA-induced calcium influx. Instead, bilobalide seems to inhibit NMDA-induced fluxes of chloride ions through ligand-operated chloride channels. In our experimen…

Calcium IsotopesMaleN-Methylaspartatemedicine.drug_classGlycineCyclopentanes44'-Diisothiocyanostilbene-22'-Disulfonic AcidIn Vitro TechniquesHippocampusChlorideCholinechemistry.chemical_compoundChloridesBilobalideFurosemideExcitatory Amino Acid AgonistsmedicineAnimalsCholineDrug InteractionsPharmacology (medical)Channel blockerRats WistarDiureticsFuransCell MembraneGeneral MedicineReceptor antagonistPyrrolidinonesRatsPsychiatry and Mental healthGinkgolidesnervous systemchemistryBiochemistryDIDSPotassiumChloride channelBiophysicsNMDA receptorCalciumDiterpenesDizocilpine MaleateExcitatory Amino Acid AntagonistsSynaptosomesmedicine.drugPharmacopsychiatry
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Cannabinoid receptor 1 modulates the autophagic flux independent of mTOR- and BECLIN1-complex

2013

Cannabinoid Receptor 1 (CB1) has been initially described as the receptor for Delta-9-Tetrahydrocannabinol in the central nervous system (CNS), mediating retrograde synaptic signaling of the endocannabinoid system. Beside its expression in various CNS regions, CB1 is ubiquituous in peripheral tissues, where it mediates, among other activities, the cell's energy homeostasis. We sought to examine the role of CB1 in the context of the evolutionarily conserved autophagic machinery, a main constituent of the regulation of the intracellular energy status. Manipulating CB1 by siRNA knockdown in mammalian cells caused an elevated autophagic flux, while the expression of autophagy-related genes rema…

Cannabinoid receptorMorpholinesGreen Fluorescent ProteinsDown-RegulationmTORC1NaphthalenesBiochemistryMiceCellular and Molecular NeurosciencePiperidinesReceptor Cannabinoid CB1RimonabantAutophagymedicineAnimalsHumansEnzyme InhibitorsCannabinoid Receptor AntagonistsCells CulturedPI3K/AKT/mTOR pathwayAdenine NucleotidesChemistryTOR Serine-Threonine KinasesAutophagyMembrane ProteinsCalcium Channel BlockersEmbryo MammalianEndocannabinoid systemBenzoxazinesCell biologyMice Inbred C57BLnervous systemAstrocytesPyrazolesBeclin-1lipids (amino acids peptides and proteins)MacrolidesSynaptic signalingRimonabantApoptosis Regulatory ProteinsFlux (metabolism)medicine.drugJournal of Neurochemistry
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WIN 55,212-2, agonist of cannabinoid receptors, prevents amyloid β1-42 effects on astrocytes in primary culture

2015

Alzheimer's disease (AD), a neurodegenerative illness involving synaptic dysfunction with extracellular accumulation of Aβ1-42 toxic peptide, glial activation, inflammatory response and oxidative stress, can lead to neuronal death. Endogenous cannabinoid system is implicated in physiological and physiopathological events in central nervous system (CNS), and changes in this system are related to many human diseases, including AD. However, studies on the effects of cannabinoids on astrocytes functions are scarce. In primary cultured astrocytes we studied cellular viability using MTT assay. Inflammatory and oxidative stress mediators were determined by ELISA and Western-blot techniques both in…

Cannabinoid receptormedicine.medical_treatmentInterleukin-1betaNitric Oxide Synthase Type IIlcsh:Medicinemedicine.disease_causeReceptors CannabinoidWIN 55212-2Receptorlcsh:ScienceCerebral CortexMultidisciplinaryCalcium Channel BlockersSistema nerviós Malaltiesmedicine.symptomSignal transductionResearch ArticleSignal Transductionmedicine.drugmedicine.medical_specialtyCell SurvivalMorpholinesPrimary Cell CultureInflammationNaphthalenesBiologyNeurologiaFetusInternal medicinemedicineAnimalsViability assayCannabinoid Receptor AgonistsAmyloid beta-PeptidesSuperoxide DismutaseTumor Necrosis Factor-alphalcsh:RTranscription Factor RelAPeptide FragmentsBenzoxazinesRatsPPAR gammaOxidative StressEndocrinologyGene Expression RegulationCyclooxygenase 2Astrocyteslcsh:QFisiologia humanaCannabinoidOxidative stress
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